EPILEPSY ,HEADACHE ,MIGRAINE Flashcards
Df and etiology of EPILEPSY
–DF:It is a disorder characterized by recurrent seizures
recurrent transient attacks of somatic, psychic, or, autonomic clinical features Represent clinical features of abnormally hypoexcitable cortical neurons, Result from paroxysmal and excessive electrical neuronal discharges ,ASSOCIATED WITH EEG changes & may be disturbance of consciousness.
–ETIOLOGY :
1. Idiopathic epilepsy : NO cause can be detected
* It is the commonest cause. ( 65 % )
* It may be associated with positive family history in some cases.
* It starts in the l st & 2nd decades in the form of:
- Grand ma! epilepsy.
- Petit mal epilepsy.
- Myoclonic epilepsy.
- Atonic seizures.
2. Secondary epilepsy : a cause can be detected
A. Local causes in the brain:
l. Congenital: cerebral palsy.
2. Traumatic: cerebral contusion or laceration.
3. Inflammatory: encephalitis, mening1t1s, brain abscess.
4. Neoplastic: brain tumours.
5. Degenerative: presenile dementia.
6. Vascular: stroke (especially hemon-hagic), hypertensive encephalopathy.
B. General causes with secondary effects on the brain:
I. Toxic: - Alcohol, cocaine, lead. - Botulism, tetanus.
2. Iatrogenic: - Lidocaine, INH. - Ambilhar, Amphetamine, Aminophylline.
3. Metabolic: - j glucose & ! glucose. - j Ca & ! Ca. - j Na & ! Na.
4. Endocrinal: - Hypoparathyroidism. - Hype1thyroid crisis.
5. Organ fai lure: - Hepatic failme. - Renal failure.
6. Heart disease: - Adam’s Stoke’s attacks. - Fallot’s tetralogy.
7. Nutritional: - Pellagra. - Vitamin B6 deficiency.
8. Physical: - High fevers. - Heat stroke.
9. HYSTERICAL.
CLINICAL PICTURE of Epilepsy GENERALISED SEIZURES ( Grand Mal Epilepsy)
I. Grand Mal Epilepsy: attacks of tonic-clonic convulsions
-it has 3 stages :
1. Pre-ictal stage : It is a warning sign of a coming attack.
-It may be:
* Somatic: Myoclonus, Parasthesias.
* Psychic: Hallucinations.
* Autonomic: Tachycardia, Sweating.
2. Ictal stage (seizure) : Sudden loss of consciousness: for seconds to minutes.
- Tonic phase (few seconds)
o The HEAD: is retracted to one side & the eye balls rolled up.
o The JAWS: are firmly clenched, with biting of the TONGUE.
o CYANOSIS: due to impaired respiration.
o There may be incontinence of urine.
- Clonic phase (few minutes) :
o The HEAD: jerks forcibly.
3. Post-ictal stage :
- It may be:
* Somatic: Todd’s paralysis(< 24 hours, due to neuronal exhaustion).
* Psychic: Confusion.
* Autonomic: Vomiting.
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Drug of choice: Carbamazepine (Tegretol) or Phenytoin (Epanutin)
CLINICAL PICTURE of Epilepsy GENERALISED SEIZURES (Petit Mal Epilepsy)
- It starts in childhood & improves at puberty & usually disappears at the age of 20
- It is NOT PRECEEDED by aura & NOT FOLLOWED by sequelae.
- It is usually PRECIPITATED by: hyperventilation or photic stimulation.
- It is characterized by: sudden loss of consciousness of short duration (few seconds).
- It may be associated with:
* High frequency ( 50 attacks / day).
* Falling to the ground without warning.
* Jerky movements of the head & UL (myoclonic petit mal).
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Drug of choice: Valproate (Depakine) or Succinimide (Zarontin)
CLINICAL PICTURE of Epilepsy GENERALISED SEIZURES
(. M oclonic Seizures/Atonic seizures)
Ill. M.oclonic Seizures: “attacks of involuntary clonic movements “
- It is characterized by: sudden, jerky, shock-like INVOLUNTARY muscle contraction.
* The jerks are bilateral contractions, mainly of the shoulders and arms.
* However, some patients report jerking in the lower limbs, trunk, or head.
- It may be of 2 types:
* Simple: - Occurs singly (no loss of consciousness).
* As a part of: - Grand mal epilepsy (aura). - Petit mal epilepsy.
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Drug of choice: Valproate (Depakine) or Clonazepam (Rivotril)
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IV. Atonic seizures:
- Transient attacks of brief loss of postural tone, often resulting in falls and injuries.
explain PARTIAL SEIZURES
-DF :Excessive electrical discharges from certain neurons in a certain area in ONE hemisphere and it have 2 types :
A. Simple seizures: “ No disturbance in consciousness “
- The seizures depends on the site of the hyperexcitable neurons in the cerebral cortex, whether in: “Motor area or Sensory areas”.
1. Motor fits:
* Focal fits: movement of part of a limb or the whole limb.
* Motor jacksonian fits: movement of one side of the body (see before).
2. General Sensory fits:
* Focal fits: parasthesia of part of a limb or the whole limb.
* Sensory jacksonian fits: parasthesia of one side of the body (see before).
3. Special Sensory fits:
* Visual hallucinations: irritation of the visual sensory area.
* Auditory hallucinations: irritation of the auditory sensory area.
* Olfactory hallucinations: irritation of the uncus.
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B. Complex seizures: “ disturbance in consciousness “
- SITE: The hyperexcitable neurons are in the Temporal lobe “Temporal lobe epilepsy”.
- DURATION: The seizure lasts few seconds to few minutes.
- The seizure starts with Aura, followed by Absence, Automatism, Amnesia
1.Aura: Olfactory hallucinations, Deja-vu phenomenon, Sensation of fear.
2.Absence:Absent patient with staring eyes (with no response to conversation).
3.Automatism:Involuntary Purposeless acts: motor ( eg, lip smacking, chewing) or verbal.
4.Amnesia:No recalling of the seizure.
explain PARTIAL SEIZURES > GENERALISED SEIZURES
Partial seizures may spread to involve the whole brain >secondarily generalised seizures “ .
explain Hysterical epilepsy
- Usually: young neurotic Sj2 .
- The cause: psychological & there is no organic lesion.
- Incidence: usually occurs in the presence of people.
- It is associated with:
- It is not associated with:
- EEG: normal.
INVESTIGATIONS
- EEG:
* It is the most specific test for epilepsy because it records the electrical activity of the brain.
* It shows specific pattern: “Epilepsy waves”. - LOCAL INVESTIGATIONS: “CT & MRI of the brain”
* To identify or exclude a LOCAL CAUSE of seizures in the brain. - GENERAL INVESTIGATIONS: “Laboratory investigations”
* To search for a GENERAL CAUSE of seizures, e.g. blood glucose.
TREATMENT
Drug /Dose / Best indicated
1. Barbiturates (Pbenonobarbitone) 100-600 mg I day
- Broad spectrum.
- Not for petit mal.\
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2. Hydantoin (Epanutin) 100-600 mg / day
- Grand mal.
- Motor Jacksonian fits.
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3. Carbamazepine 200-600 mg I day
- Grand mal.
- Motor Jacksonian fits.
- Complex seizures.
- Not for petit ma!.
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4. Clonazepam 2-6 mg I day
- Myoclonic.
- Grand mat.
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5. Valproate 500-1500 mg I day - Broad spectrum.
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6. Succinamide 500-1000 mg / day - Petit mat.
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NEW ANTI-EPILEPTIC DRUGS
- These drugs are new dtugs that may be used in resistant seizures.
1. Lamotrigine: 200 - 400 mg / day.
2. Felbamate: 400 - 800 mg / day.
3. Gabapentin: 600 - 1200 mg / day.
explain STATUS EPILEPTICUS DF/Treatment
- A medical emergency:
1. Repeated attacks of generalized convulsions, with lack of recove,y of consciousness, OR,
2. Persistent attack of seizure lasting for at least 30 minutes. - If the convulsions are not stopped rapidly, coma deepens & death may occur due to: heart failure or respiratory failure or brain damage or hyperpyrexia.
- The most common causes are: sudden withdrawal of anti-epileptic drugs & stroke.
——————-TREATMENT:
-Specific Treatment: - Phenytoin with diazepam (or clonazepam) immediately
-If seizures persist after 20 min. of Phenytoin & diazepam:
. PHENOBARBITONE: 200 mg infusion. - In resistant cases: GENERAL ANAESTHESIA: may be used.
DF , ETILOGY AND TYPES OF HEADACHE
-DF: Mild to severe pain in the head including the FRONT of the face & the BACK of the head.
-ETIOLOGY & TYPES:
1. Vascular headache: due to Vascular dilatation or Vasculitis
a) Primary: MIGRAINE, Cluster headache, Temporal arteritis
b) Secondary:
* Hypertension.
* Hypoxia.
* Hypoglycemia.
* Drugs causing VD: e.g. Nitrates.
* Toxins causing VD: Alcohol, Infections (bacterial or viral toxins).
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2. Inflammation:
* Intracranial: Meningitis, Encephalitis.
* Neuritis: of the sensory nerves of the scalp: e.g. Trigeminal neuralgia.
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3. Traction headache: due to stretch of the meninges, increase ICT
* Brain tumor, abscess, or hemorrhage. * Post-lumbar puncture.
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4. Muscle contraction headache: When one gets a “ STIFF NECK,” the prolonged muscle spasm can compress the nerves
and also induce ischemia. with production of metabolites which stimulate pain receptors:
* Prolonged driving. * Cervical spondylosis.
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5. Referred headache: due to diseases i1l different parts of the head
* Eyes: e.g. glaucoma.
* Ears: e.g. ear infections
* Nose: e.g. sinusitis
* Mouth: e.g. dental sepsis.
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6. Tension headache (Psychogenic): “the most common cause”
* It occurs in: psychologically distmbed persons usually FEMALES.
* It occurs as: pressure or BAND-LIKE, Bilateral fronto-occipital
DF , ETILOGY AND incidence , types OF MIGRAINE
-DF :- It is a paroxysmal disorder characterized by intense throbbing headache, (usually unilateral) associated with autonomic manifestations, e.g. nausea & vomiting.
-Etiology :
* Idiopathic.
* GENETIC: Hereda-familial ( 80 % ).
-incidence:
* SEX: more in young FEMALES ( female / male = 3 / 1 ).
* RESIDENCE: more in urban areas.
* PERSONALITY: more in perfectionistic people.
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-Types :
1. CLASSIC migrame (25 %): always preceded by aura.
2. COMMON migraine (75 %): not preceded by aura; probably due to mild VC stage.
3. RARE VARIANTS:
* Hemiplegic migraine: associated with transient hemiplegia.
* Facial migraine: associated with transient facial paralysis.
* Retinal migraine: associated with transient decreased vision.
explain MIGRAINE TRIGGERS “4 M “
- Mental & physical exertion.
- Menses.
- Medications: Vasodilators (nitrates), CCPs.
- Meals (& … .. ): Cheese, Chocolate, Citrus fruits .
Smoking, Alcohol.
CLINICAL PICTURE of Migraine ( 2 stages )
- First stage: “ Aura “
* Visual: Flashes of light or blind spots.
* Sensory: Paresthesia.
* Motor: Weakness.
——————— - Second stage: “ Migraine “
It occurs in periodic & recurrent attacks:
* SITE & REFERENCE: Starts in the temple or around the eye & then:
speared to involve the whole side of the head.
* CHARACTER Pulsating or Throbbing.
* DURATION: It lasts for few hours to few days (3hours to 3 days).
* AGGRAVATED BY: Bright light, Physical & Emotional stress.
* RELIEVED BY: Sleep.
* ASSOCIATIONS: Nausea, vomiting, Photophobia, Phonophobia.
PATHOGENESIS of Migraine
- NEUROVASCULAR THEORY
A) VASOACTIVE NEUROPEPTIDES
* Migraine triggers - abnormal overexcitation of Trigeminal nerve axons
- release of V ASOACTIVE NEUROPEPTIDES including Substance P
from Trigeminal nerve endings (near the meningeal blood vessels).
B) VASODILATATION + STERILE INFLAMMATION
* These peptides will cause: VD + STERILE INFLAMMATION at the
Trigeminal nerve endings that spreads to the nearby meninges.
C) PAIN results due to both VD & INFLAMMATION.
!Serotonin through acting on its receptors appears to block these peptides!
————————– - SEROTONIN THEORY
Initially: An initial increase in plasma serotonin levels will cause constriction of cerebral blood vessels and a reduction in cerebral blood flow –+ AURA.
Later: A subsequent drop in plasma serotonin levels will then lead to marked dilation of the arteries –+ HEADACHE of MIGRAINE.
———- - DOPAMINE THEORY
Recently: abnormal Dopaminergic stimulation - HEADACHE of MIGRAINE, and also causes associated manifestations such as nausea & vomiting.
